期刊
JOURNAL OF VIROLOGY
卷 82, 期 11, 页码 5398-5407出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.02176-07
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资金
- NCRR NIH HHS [UL1 RR024131-01, UL1 RR024131] Funding Source: Medline
- NIAID NIH HHS [U01 AI043864, AI43864, R01 AI047062, AI44595, AI055273, AI057020, R01 AI052745, R01 AI044595, R21 AI055273, AI47062, AI052745, R01 AI057020, R01 AI043864] Funding Source: Medline
- NIH HHS [DP1 OD000329] Funding Source: Medline
- NIMH NIH HHS [P30 MH62246, P30 MH062246] Funding Source: Medline
A rare subset of human immunodeficiency virus (HIV-infected individuals maintains undetectable HIV RNA levels without therapy (elite controllers). To clarify the role of T-cell responses in mediating virus control, we compared HLA class I polymorphisms and HIV-specific T-cell responses among a large cohort of elite controllers (HIV-RNA < 75 copies/ml), viremic controllers (low-level viremia without therapy), non-controllers (high-level viremia), and antiretroviral therapy suppressed individuals (undetectable HIV-RNA levels on antiretroviral therapy). The proportion of CD4(+) and CD8(+) T cells that produce gamma interferon (IFN-gamma) and interleukin-2 (IL-2) in response to Gag and Pol peptides was highest in the elite and viremic controllers (P < 0.0001). Forty percent of the elite controllers were HLA-B*57 compared to twenty-three percent of viremic controllers and nine percent of noncontrollers (P < 0.001). Other HLA class I alleles more common in elite controllers included HLA-B*13, HLA-B*58, and HILA-B*81 (P < 0.05 for each). Within elite and viremic controller groups, those with protective class I alleles had higher frequencies of Gag-specific CD8(+) T cells than those without these alleles (P = 0.01). Noncontrollers, with or without protective alleles, had low-level CD8(+) responses. Thus, certain HLA class I alleles are enriched in HIV controllers and are associated with strong Gag-specific CD8(+)IFN-gamma+IL-2(+) T cells. However, the absence of evidence of T cell-mediated control in many controllers suggests the presence of alternative mechanisms for viral control in these individuals. Defining mechanisms for virus control in non-T-cell controllers might lead to insights into preventing HIV transmission or preventing virus replication.
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